ReviewClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2026
Cancer metabolism: bridging tumorigenesis mechanisms to treatment susceptibility.
Review in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Cellular metabolism has emerged as a pivotal factor influencing the viability and functionality of cancer cells. To satisfy their substantial anabolic requirements, tumor cells adopt a distinct metabolic reprogramming divergent from that of non-transformed somatic cells. This review aims to examine metabolic reprogramming in head and neck squamous cell carcinoma (HNSCC), examining its role as a fundamental aspect of cancer progression and resistance to treatment. The article systematically summarizes the key mechanisms of metabolic reprogramming in HNSCC, including enhanced glycolysis, remodeling of amino acid metabolism, and dysregulation of lipid synthesis, and discusses how these metabolic pathways facilitate tumor proliferation and metastasis by influencing the microenvironment, antioxidant defenses, and resistance to ferroptosis. Additionally, the review examines the dynamic interactions between metabolic reprogramming and the tumor microenvironment, particularly focusing on HIF-1α-driven metabolic adaptation and immune evasion mechanisms under hypoxic conditions. Finally, the potential of metabolic-targeted therapies is discussed, highlighting future research directions and their applications in personalized treatment strategies.
Indexed as
Identifiers
41016996What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.